Evidence map›Paper›PMID 17875987›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Tumor-suppressive miR-34a induces senescence-like growth arrest through modulation of the E2F pathway in human colon cancer cells.

Hiroshi Tazawa, Naoto Tsuchiya, Masashi Izumiya, Hitoshi Nakagama

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 456 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
456citing papers in PubMed, 2 pooled it
27.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

456 citing papers in PubMed, 2 syntheses or guidelines pooled it, 901 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Molecular insight into the therapeutic potential of miR-34a in retinoblastoma.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  6. Review
  7. Sperm abnormality: Differential expression of microRNAs.Journal of assisted reproduction and genetics · 2025
    Review
  8. Review
  9. Dysregulated miRNAs Targeting Adiponectin Signaling in Colorectal Cancer.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Identification of Oncogene-Induced Senescence-Associated MicroRNAs.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  17. Article
  18. Review
  19. Article
  20. Article

396 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Hiroshi TazawaBiochemistry Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
Naoto Tsuchiya
Masashi Izumiya
Hitoshi Nakagama
National Cancer Centre Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence suggests a role for microRNAs in human carcinogenesis as novel types of tumor suppressors or oncogenes. However, their precise biological role remains largely elusive. In the present study, we aimed to identify microRNA species involved in the regulation of cell proliferation. Using quantitative RT-PCR analysis, we demonstrated that miR-34a was highly up-regulated in a human colon cancer cell line, HCT 116, treated with a DNA-damaging agent, adriamycin. Transient introduction of miR-34a into two human colon cancer cell lines, HCT 116 and RKO, caused complete suppression of cell proliferation and induced senescence-like phenotypes. Moreover, miR-34a also suppressed in vivo growth of HCT 116 and RKO cells in tumors in mice when complexed and administered with atelocollagen for drug delivery. Gene-expression microarray and immunoblot analyses revealed down-regulation of the E2F pathway by miR-34a introduction. Up-regulation of the p53 pathway was also observed. Furthermore, 9 of 25 human colon cancers (36%) showed decreased expression of miR-34a compared with counterpart normal tissues. Our results provide evidence that miR-34a functions as a potent suppressor of cell proliferation through modulation of the E2F signaling pathway. Abrogation of miR-34a function could contribute to aberrant cell proliferation, leading to colon cancer development.

Indexed as

Cellular SenescenceGene Expression Regulation, NeoplasticAnimalsCell Line, TumorCell ProliferationCollagenDoxorubicinE2F Transcription FactorsHumansMiceMicroRNAsNeoplasm TransplantationPhenotypeTumor Suppressor Protein p53CollagenDoxorubicinE2F Transcription FactorsMicroRNAsMIRN34 microRNA, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID17875987
PMCPMC2000550
OpenAlexW2074210527

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.